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Pharmacology > Type II DM > Flashcards

Type II DM Flashcards

1
Q

Which cells of the pancreas release insulin and amyline?

A

beta cells

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2
Q

Which cells of the pancreas release glucagon?

A

alpha cells

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3
Q

Name 3 rapid insulin analogs?

A

Glulisine, Asport and Lispro
P: 30 min
D: 5 hrs

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4
Q

Name 1 short acting insulin analog?

A

Insulin
P: 2 hrs
D: <8 hr

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5
Q

Name 1 intermediate insulin analog?

A

NPH
P: 6 hrs
D: 18 hrs

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6
Q

Name 3 long acting insulin analogs?

A

Detemir
Glargine
Degludec

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7
Q

How is the biochemistry altered to achieve long acting insulin products

A

Detemir: FA side chains added to bind albumin and cause a slower release
Glargine: less soluble at neutral pH= decreased absorption
Degludec: forms long chains of hexamers causing slower absorption and continuous release

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8
Q

What is the duration of action of each long acting insulin?

A 
Glargine:
P:0
D: 24hrs
Degludec
P:0
D: >24 hrs
Detemir: 
P: 6 hrs
D: 24 hrs
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9
Q

How was the biochemistry altered to produce rapid acting insulin?

A

biochemistry altered to decreased heameric aggregation of insulin

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10
Q

How was the biochemistry altered to achieve intermediate acting insulin (NPH)?

A

protamine and zinc added to form a precipitate in subQ tissues to delay absorption and produce a longer lasting insulin

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11
Q

What are ADE of insulin analogs? (5)

A
  • HYPOGLYCEMIA -(higher risk with human insulin or NPH vs analogs)
  • lipodystrophy at site of injection
  • weight gain
  • CHF risk
  • renal effects: lower insulin doses required with decreased eGFR
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12
Q

What is the role of amyline/pramlintide?

A
  • decrease gastric emptying
  • decrease postprandial glucagon
  • increase satiety
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13
Q

What is the clinical application of pramlintide? ADE?route?

A

-allows insulin synthetic doses to be reduced
ADE: weight loss, nausea, hypoglycemia
route: injectable

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14
Q

What is MOA of incretins?

A

eating/food stimulates the release of incretin

(GLP-1 or GIP) hormones from the gut and incretins work by stimulating the pancreas to release more insulin

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15
Q

What are the two incretin molecules?Name the 2 diabetic drugs that are incretin mimetics?route of delivery?

A
  • GLP-1 and GIP
  • Exenatide and Liraglutide
  • injectable
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16
Q

What is the role of incretin mimetics?

A
  • decrease gastric emptying
  • increase insulin
  • increase satiety
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17
Q

What are the ADE of incretin mimetic? (4)

A
  • weight loss
  • N/V/D, constipation, GI sx
  • exenatide not used when CrCl < 30
  • Black box: thyroid c-cell tumor
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18
Q

What is MOA of DPP4-I?

A

they block the enzyme DPP4 to prevent metabolism of GLP1 and GIP

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19
Q

Name 4 DPP4-I? What is route of delivery?

A

Alogliptin, Linagliptin, saxagliptin, sitagliptin,

Route: oral

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20
Q

Which DPP4-I does not need renal dose adjustment? Which cause CHF?

A
  • Linagliptin

- saxagliptin and alogliptan

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21
Q

What are ADE of DPP4-I?

A

acute pancreatitis
joint pain
nasopharyngitis
HA

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22
Q

What is the role of DPP4-I?

A

decrease glucagon
increase insulin
decrease gastric emptying

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23
Q

What is MOA of sulfonylureas?

A
  • binds and inhibits ATP/K sensitive channel causing depolarization and triggering release of insulin
  • decrease glucose production in the liver
  • increases sensitivity of beta cells to glucose
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24
Q

Glimepride, Glyburide, and Glipizid are what class of diabetic drugs?

A

sulfonylureas

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25
Q

What are ADE of SU? (4)

A

hypogylcemia
weight gain
cardiovascular mortality
wide drug-drug interactions

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26
Q

What class of drugs are Nateglinide and Repaglinide?

A

Glinides

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27
Q

What is MOA of glinides?

A

they bind the ATP/K channels but at a different location than the SU
-they are more rapid with a shorter duration of action when compared to SU

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28
Q

What is the clinical use of glinides?

A

useful for post prandial hyperglycemia

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29
Q

What are ADE of glinides?

A
  • hypoglycemia
  • weight gain
  • less risk than SU
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30
Q

What drug class is metformin?

A

Biguanides

31
Q

What is MOA of biguanides?

A
  • decreases liver glucose production
  • increase peripheral insulin activity
  • decreases glucose absorption in the gut
32
Q

What are ADE of biguanides? (5)

A
  • moderate weight loss
  • contraindicated in eGFR<30
  • N/V/D
  • lactic acidosis
  • B12 deficiency
33
Q

What drug class are Proglitazone and Rosiglitazone?

A

Thiazolidinedione (TZD)

34
Q

What is MOA of TZD?

A
  • binds DNA and expresses and suppresses certain genes
  • increase insulin sensitivity in adipose tissue, SM, liver
  • decreases liver glucose production
  • increase fatty acid utilization in adipocytes which helps increase insulin and glucose uptake
35
Q

What are ADE of TZD? (7)

A 
weight gain
fluid retention -don't use in pts with renal issues 
increase LDL
increase HDL 
Black box: CHF 
risk of bone fx 
bladder cancer for proglitazone
36
Q

What drug class are Canagliflozin and Dapagliflozine?

A

SGLT2-I

37
Q

What is MOA of SGLT2-I

A

PCT in kidney is blocked to stop glucose reabsorption iincrease glucose in urine

38
Q

What are ADE of SGLT2-I? (11)

A

-weight loss
-renal dose adjustment required
-contraindicated with eGFR <45
black box: risk of amputation
-genital mycotic infections
-hypotension
-increased LDL cholesterol
-risk of Fourier’s gangrene
-thirst
-urination
-UTI

39
Q

What drug class is Acarbose and Miglitol?

A

alpha glucosidase inhibitors

40
Q

What is MOA of alpha glucosidase inhibitors

A

blocks alpha glucosidase in GI brush border to decrease absorption of glucose and decrease postprandial glucose levels

41
Q

What are ADE of alpha-glucosidase inhibitors?

A

flatulence, abdominal cramps, bloating, diarrhea

42
Q

which diabetic drug has risk of hypoglycemia?

A

insulin

SU

43
Q

Which diabetic drugs cause weight loss?

A

metformin
SGLT2-I
GLP-1RA

44
Q

Which diabetic drugs have ASCVD benefit?

A
  • TZD-reduces tsroke risk but not CHF
  • metformin
  • SGLT2-I
  • GLP-1RA
45
Q

Which diabetic drugs have HF risk?

A

TZD

DPP4-saxagliptin

46
Q

T/F Metformin is contraindicated in eGFR <30

A

True

47
Q

Which drug class is does not require renal dose adjustment?

A

TZD

48
Q

What is first line therapy for type II DM according to ADA?

A

metformin and lifestyle change( weight and physical activity

49
Q

What drug is added/choosen if patient has ASCVD risk according to ADA?

A

GLP-1RA
or
SGLT2-i

50
Q

What is 3rd line for ASCVD risk?

A
  • basal insulin
  • TZD
  • SU
  • DPP-4
51
Q

What can be added to metformin with patients who have CKD?

A

SGLT2-i

52
Q

What should you consider before injectable insulin therapy?

A

GLP1 injection

53
Q

What is insulin intensifying therapy first line medication?

A

basal insulin

54
Q

what do you add if basal insulin is insufficient to lower A1C?

A

add prandial insulin

55
Q

Which oral diabetic drugs are the cheapest?

A

biguanides and SU

56
Q

What are the 4 lifestyle therapies recommended by the AACE?

A

-nutrition
–physical activity-150 min exercise/day
behavior modifications: reduce alcohol, see HCP for mood
-smoking cessation

57
Q

If a patient with pre-diabetes progresses to overt diabetes what tx do you initiate first?

A
  • metformin or Acarbose , if after initiating tx is still persist add GLP1-RA
  • intensify weight loss therapy
58
Q

What weight loss drugs are recomended by AACE?

A

Liragluitde 3mg, Lorcaserin, orlistat or bariatric surgery

59
Q

How do you treat HTN and and diabetes per AACE?

A

If BP >150/100: give ACE/ARB with CCB/thiazide/BB

For elevated BP: start with ACE/ARB, reassess in 2-3 months, if not at goal (goal SBP <130, DBP <80) add CCB/BB/Thiazide

60
Q

What is the first step in mgmt in a patient with dyslipidemia and diabetes?

A
  • initiate/intensify lifestyle changes
  • assess ASCVD risk
  • initiate statin therapy
  • add fenofibrate or RX Omega 3FA for TG >500
61
Q

What are the goals for a patient with dyslipidemia and diabetes in the high risk category?

A

LDL: <100
non -HDL: <130
TG: <150
Apo B: <90

62
Q

What are the goals for a patient with dyslipidemia and diabetes in the very high risk category?

A

LDL: <70
non HDL: <100
TG: <150
Apo B: <80

63
Q

What are the goals for a patient with dyslipidemia and diabetes in the extreme category?

A

LDL: <55
non HDL: <80
TG: <150
Apo B: <70

64
Q

What meds can you use to lower the LDL-C?

A

-intensify statin, or add ezetimibe, PCSK9i, colveselam, niacin

65
Q

What meds can you use to lower TGA?

A

add fenofibrate or RX Omega 3FA f

66
Q

What meds can you use to lower Apo-B?

A

-intensify statin, or add ezetimibe, PCSK9i, colveselam, niacin

67
Q

What meds can you use to lower LDL in patients with Familial hypercholesteremia?

A

statin + PCSK9i

68
Q

If patient presents with entry A1C of <7.5% what is drug of choice?

A

metformin
GLP-1RA
SGLT2i

69
Q

If patient presents with entry A1C of 7.5-9.0% what drug do you initiate?

A

SGLT or GLP-1RA with metformin-dual therapy

if after 3 months AIC is still elevated use triple therpay with met +GLP+SGLT2i

70
Q

If patient present with A1C of >9% but has no symptoms what meds do you give?

A

SGLT or GLP-1RA with metformin-dual therapy
or
triple therapy with met +GLP+SGLT2i

71
Q

If patient present with A1C of >9% and has symptoms what meds do you give?

A

insulin therapy wiht other therapies

72
Q

When initiating insulin therapy what class of insulin do you use?

A

Basal insulin

use long acting

73
Q

If the patient has begun insulin therapy but hyperglycemia persist, what drugs can you initiate?

A
  • if not already on GLP-1RA start this

- use prandial insulin( rapid acting) before largest meal or before each meal

74
Q

If after adding prandial insulin but hyperglycemia persist what therapy can you use?

A

basal bolus-give additional basal dose and prandial insulin before each meal
or

Pharmacology (47 decks)

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